properties of cancer (W13) Flashcards

1
Q

epithelial malignancy name?

A

carcinoma

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2
Q

which part of an ulcer should you biopsy

A

the edge

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3
Q

appearances of surface neoplasms?

A

plaque, ulcerated, annular, pedunculated polyp, papillary, exophytic/mass forming

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4
Q

difference between polyp and papillary

A

polyp - epithelium covers raised core
papillary - epithelium covers thin branches. greater surface area but same size

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5
Q

name for neoplasm with connective tissue stalk?

A

pedunculated

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6
Q

name for neoplasm without connective tissue stalk?

A

sessile

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7
Q

benign neoplasms - how do they cause problems?

A

compression
obstruction/intussusception
haemorrhage, infarction
secreted products
progression to malignancy
cosmetic
local trauma/irritation

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8
Q

problems with neoplasms which are tubes/ducts/surfaces

A

perforation, occlusion, ulceration

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9
Q

problems with neoplasms which are space -occupying

A

spinal cord compression

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10
Q

problems with neoplasms - organ destruction?

A

liver failure from carcinomatosis, CNS invasion

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11
Q

problems with neoplasms - organ encasement?

A

respiratory failure (pleural mesothelioma)

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12
Q

cachexia?

A

muscle goes into catabolic mode, ‘cannibalises itself’, not reversable with nutritional support

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13
Q

paraneoplastic meaning?

A

usually secretion of factors from neoplasms that the tissue wouldn’t usually secrete

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14
Q

paraneoplastic complications

A

venous thrombosis
hypercalcaemia
neuropathies
dermatomycosis
finger clubbing
nephrotic syndrome

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15
Q

field cancerisation?

A

expanded collections of cells that express some positively selected phenotypic changes needed for malignancy

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16
Q

clonal mosaicism?

A

cells with genes with a survival advantage in a tissue expands a the expense of others resulting in a less diverse cell population in a tissue.

17
Q

what does mutation count and clone size increase with

A

chronic inflammation
carcinogens (sun exposure, smoking, alcohol)

18
Q

how does chronic inflammation cause an increase in mutation count and clone size

A

more regeneration, more DNA damage

19
Q

how do carcinogens cause an increase in mutation count and clone size

A

many chemical carcinogens do not mutate, but enable clonal expansion

20
Q

how many altered driver genes is needed to convert a normal cell to an early invasive cancer cell

A

around 3 - varies with cancer type and individuals

21
Q

what many cancerous tissues look like?

A

normal
hyperplastic (too many cells)
metaplastic
dysplastic (cells look weird - highest risk)

22
Q

clonal haematopoiesis?

A

driver gene mutations in bone marrow favour growth of bone marrow cells. cases white blood cells produced to be more inflammatory

23
Q

clonal haematopoiesis is a risk factor for which diseases

A

coronary heart disease, stroke, chronic liver disease

24
Q

where are vessels present in a cancer? what does this cause?

A

only on the outer parts, at some point as you get deeper the tissue pressure is too high. This causes tissue fluid to seep to the surface towards lymphatics (allowing any detached cancer cells to easily spread)

25
acidity of a cancer tumor
pretty acidic as there is not much glucose or oxygen
26
why is the outwards movement of tissue fluid in a cancer problematic for treatment
drugs aren't likely to diffuse in, will only effect the surface of the cancer
27
characteristic of fast growing cancer
viable cells around blood vessels and necrosis in-between
28
what does chaotic angiogenesis create
chaotic blood flow (so silly so goofy) pooling, eddies, flow reversals, leakiness etc. creates regional differences within a cancer
29
what happens when cancer driver genes are multiply copied? what does this mean?
copies tend to detach from the chromosome and form a ring (similar to a bacterial chromosome) this causes it not to be picked up in whole gene sequencing
30
universal cancer tasks
division, accumulation of biomass, lipogenesis, immune interaction, invasion and tissue remodelling
31
cancer trade off between conflicting tasks causes what?
cancers have to have plasticity to alter trade-offs between tasks
32
mesenchymal plasticity?
carcinoma can reversibly take on characteristics of fibroblasts
33
what does epithelial mesenchymal plasticity (EMP) allow cancer cells to do
move and therefore invade downregulate proliferation therefore resist therapy that targets proliferating cells
34
how do metabolic conditions in cancer impair the immune system
antigen signalling under metabolic stress causes CD8 T cell exhaustion. cancer cells very good at stealing all the glucose.
35
what eliminates most circulating cancer cells
NK cells
36
how do cancer cells subvert immune activation
release immunosuppressive factors. repress antigen processing and presentation. reduce MHC 1 display immune inhibitors
37
how do cancer cells survive treatment
cancer treatments leave residual cells - reservoir for relapse active resistant of treatment genetic resistance - new clone develops